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Walter Malorni

Researcher at Istituto Superiore di Sanità

Publications -  371
Citations -  39681

Walter Malorni is an academic researcher from Istituto Superiore di Sanità. The author has contributed to research in topics: Apoptosis & Programmed cell death. The author has an hindex of 69, co-authored 363 publications receiving 33990 citations.

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Gender-related differences in dietary habits

TL;DR: The European Commission has evidenced the need to combine the knowledge on sex-driven response to nutrients with that on gender-related dietary choices in order to design tailored preventive interventions aimed at effectively promoting healthy lifestyles.
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Autophagy as a pathogenic mechanism and drug target in lymphoproliferative disorders

TL;DR: In this review, the critical implications of autophagy in the pathogenesis, progression, and treatment of lymphoproliferative disorders are recapitulate.
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Adenosine- and 2-chloro-adenosine-induced cytopathic effects on myoblastic cells and myotubes: involvement of different intracellular mechanisms

TL;DR: Adenosine and 2-chloro-adenosine induce apoptosis of myogenic cells via completely different metabolic pathways, and are consistent with the hypothesis that adenosine accumulation in dystrophic muscles may represent a novel pathogenetic pathway in muscle diseases.
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Oxidized Low-Density Lipoproteins Affect Natural Killer Cell Activity by Impairing Cytoskeleton Function and Altering the Cytokine Network

TL;DR: Exposure of mitogen-stimulated peripheral blood mononuclear cells to ox-LDL markedly reduced specific mRNA transcription and release of cytokines relevant for NK cell activity (such as tumor necrosis factor-alpha, interferon gamma, and interleukin 12), which suggest that the impairment ofNK cell activity by ox- LDL likely reflects the concomitant dysregulation of some essential mechanisms of NK cell function.
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Autoantibodies specific to D4GDI modulate Rho GTPase mediated cytoskeleton remodeling and induce autophagy in T lymphocytes

TL;DR: It is concluded that anti-D4GDI autoantibodies could be capable of triggering important responses in T cells such as cytoskeleton remodeling and autophagy pathway and that, in SLE patients, the chronic exposure to these specific autoantibia could lead to the selection of Autophagy-resistant T cell clones contributing to the pathogenesis of the disease.